While the exact mechanics of compensatory hyperactivity are not
known, the phenomenon exists without a doubt in regard to sweating. Thus
we can suppose that, whatever the mechanism, other sympathetically
innervated effectors in the still-innervated zone may exhibit a similar
hyperactive response, especially if those effectors are similar to sweat
glands in that they are either
- distributed throughout the innervated and denervated areas and/or
- innervated only by the SNS, and not the PSNS
Blood vessels are distributed throughout the body, and most of them
have only sympathetic innervation. Adipose Tissue is also widely
distributed. Will either of these exhibit compensatory hyperactivity in
the still-innervated areas? If so, what would sympathetic hyperactivity
cause?
The kidneys are thought to only have sympathetic innervation, not
parasympathetic. They are expected to remain fully innervated after
ETS, but could they experience sympathetic hyperactivity? If so, how
might that affect their function?
